Our data shows that the expression of CCL2, a well known target of NF-κB p65 and a potent regulator for PCa cell migration and proliferation [31], [32], [33], can be dramatically inhibited by Celastrol at both mRNA and protein level, which provides further evidence suggesting that Celastrol may have strong biological effects on the T/E fusion expressing PCa cell growth and/or invasion by targeting downstream targets of NF-κB signal. Here, CCL2 is linked to posterior cortical atrophy.